Regulatory effect of curcumin on p300 and HDAC1 in B-NHL cells.
- Author:
Qing WU
1
;
Yan CHEN
;
Xing-Gang LI
;
Yuan-Yan TANG
Author Information
1. Institute of Hematology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
- Publication Type:Journal Article
- MeSH:
Antineoplastic Agents;
pharmacology;
Apoptosis;
drug effects;
Cell Proliferation;
drug effects;
Curcumin;
pharmacology;
Dose-Response Relationship, Drug;
E1A-Associated p300 Protein;
biosynthesis;
genetics;
Histone Deacetylase 1;
Histone Deacetylases;
biosynthesis;
genetics;
Humans;
Lymphoma, B-Cell;
metabolism;
pathology;
RNA, Messenger;
biosynthesis;
genetics;
Tumor Cells, Cultured
- From:
Journal of Experimental Hematology
2006;14(2):293-297
- CountryChina
- Language:Chinese
-
Abstract:
The purpose of this study was to investigate the effect of curcumin on proliferation of B-NHL Raji cell line and explore the relationship between this effect and regulatory expression of p300 and HDAC1 transcription. The in vitro cultured Raji cells were treated with curcumin at various concentrations (6.25-50 micromol/L) and at different time points (0, 6, 12, 24 and 48 hours), the inhibitory ratio of cell growth was measured by MTT assay, the cell apoptosis rate was detected by flow cytometry with Annexin V-FITC/PI double staining, the changes of p300 and HDAC1 mRNA expression and protein level in Raji cells were determined by RT-PCR and Western blot. The results showed that the curcumin could inhibit Raji cell proliferation in significant time-and concentration-dependent manners, IC50 at 24 hours was 25 micromol/L; the curcumin could induce apoptosis of Raji cells in concentration-dependent manner, apoptosis rate was 14.38%-61.18%. The curcumin significantly inhibited activity and expression of p300 and HDAC1. At IC50 concentration, expression of p300 and HDAC1 mRNA and protein level decreased with time-dependent manner, difference between tested and control groups was significant (P < 0.05). It is concluded that the curcumin can inhibit proliferation of B-NHL Raji cells and promote apoptosis of those cells. Curcumin can inhibit the activity and expression of the transcriptional co-activator p300 and HDAC1, which may be involved in its pharmacological mechanisms on B lymphoma cells.
